In the cathetarization laboratory, no-reflow may be clinically silent or appear suddenly associated with severe chest pain, ischemic (EKG) changes, conduction abnormalities, and/or hemodynamic deterioration. This needs to be distinguished from slow-flow which can be caused by coronary dissection, macrothrombus formation, coronary vasospasm, or distal macroembolization. The presence of no-reflow is clinically important as its presence has been associated with a five to ten fold increase in mortality,^[1] as well as a high incidence of myocardial infarction (MI), left ventricular dysfunction, ventricular arrhythmias, early congestive heart failure and cardiogenic shock. Predictors of outcome include:

• Duration of coronary occlusion
• Extent of myocardium supplied by the occluded artery
• Patency of infarct-related artery
• Quality of collateral circulation
• Presence of pre-infarction angina which produces a preconditioning-like effect and might correlate with preservation of collateral circulation.

Hyperglycemia in acute myocardial infarction is associated with an increased risk of in-hospital mortality, as well as no-reflow phenomenon.

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